Methods for Measuring Brain Mitochondrial Impairment and Oxidative Stress in Hepatic Encephalopathy
摘要
Hepatic encephalopathy (HE) is a clinical situation that refers to neurological complications of liver failure and hyperammonemia. Ammonia (ammonium ion in biological fluids; NH4+) is the primary culprit of brain injury in HE. Although the precise mechanism of NH4+-induced neurotoxicity is far from clear, it has been well-established that this chemical can induce significant oxidative stress in the brain. At subcellular levels, mitochondria are critical targets for NH4+ cytotoxicity. Therefore, potential therapeutic approaches in HE targeted oxidative stress and mitochondrial impairment. Hence, developing convenient, reliable, and reproducible methods is crucial for assessing and monitoring therapeutic interventions in HE. In the current protocol, an animal model of acute HE is described. Then, techniques for evaluating oxidative stress biomarkers in the brain, isolating brain mitochondria, and assessing mitochondrial indices are outlined.